RapamycinFungusV1, Main, Exploration, bibRecord, 001131

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.

Identifieur interne : 001131 ( Main/Exploration ); précédent : 001130; suivant : 001132

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.

Auteurs : James A. Mccubrey [États-Unis] ; Linda S. Steelman ; William H. Chappell ; Stephen L. Abrams ; Richard A. Franklin ; Giuseppe Montalto ; Melchiorre Cervello ; Massimo Libra ; Saverio Candido ; Grazia Malaponte ; Maria C. Mazzarino ; Paolo Fagone ; Ferdinando Nicoletti ; Jörg B Secke ; Sanja Mijatovic ; Danijela Maksimovic-Ivanic ; Michele Milella ; Agostino Tafuri ; Francesca Chiarini ; Camilla Evangelisti ; Lucio Cocco ; Alberto M. Martelli

Source :

Oncotarget [ 1949-2553 ] ; 2012.

RBID : pubmed:23085539

Descripteurs français

English descriptors

KwdEn :
- Antineoplastic Agents (therapeutic use), Cell Line, Tumor (MeSH), Drug Resistance, Neoplasm (MeSH), Extracellular Signal-Regulated MAP Kinases (antagonists & inhibitors), Extracellular Signal-Regulated MAP Kinases (genetics), Humans (MeSH), MAP Kinase Kinase Kinases (antagonists & inhibitors), MAP Kinase Kinase Kinases (genetics), Mutation (genetics), Neoplasms (drug therapy), Neoplasms (genetics), Neoplasms (pathology), PTEN Phosphohydrolase (antagonists & inhibitors), PTEN Phosphohydrolase (genetics), Phosphatidylinositol 3-Kinases (genetics), Phosphoinositide-3 Kinase Inhibitors (MeSH), Proto-Oncogene Proteins B-raf (antagonists & inhibitors), Proto-Oncogene Proteins B-raf (genetics), Proto-Oncogene Proteins c-akt (antagonists & inhibitors), Proto-Oncogene Proteins c-akt (genetics), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics), ras Proteins (antagonists & inhibitors), ras Proteins (genetics).
MESH :
- chemical , antagonists & inhibitors : Extracellular Signal-Regulated MAP Kinases, MAP Kinase Kinase Kinases, PTEN Phosphohydrolase, Proto-Oncogene Proteins B-raf, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, ras Proteins.
- chemical , genetics : Extracellular Signal-Regulated MAP Kinases, MAP Kinase Kinase Kinases, PTEN Phosphohydrolase, Proto-Oncogene Proteins B-raf, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, ras Proteins.
- chemical , therapeutic use : Antineoplastic Agents.
- drug therapy : Neoplasms.
- genetics : Mutation, Neoplasms, Phosphatidylinositol 3-Kinases.
- pathology : Neoplasms.
- Cell Line, Tumor, Drug Resistance, Neoplasm, Humans, Phosphoinositide-3 Kinase Inhibitors, Signal Transduction.

Abstract

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.

DOI: 10.18632/oncotarget.659
PubMed: 23085539
PubMed Central: PMC3717945

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 001096
to stream Main, to step Curation: 001096

Le document en format XML

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<author><name sortKey="Maksimovic Ivanic, Danijela" sort="Maksimovic Ivanic, Danijela" uniqKey="Maksimovic Ivanic D" first="Danijela" last="Maksimovic-Ivanic">Danijela Maksimovic-Ivanic</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.</title>
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<author><name sortKey="Chappell, William H" sort="Chappell, William H" uniqKey="Chappell W" first="William H" last="Chappell">William H. Chappell</name>
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<author><name sortKey="Abrams, Stephen L" sort="Abrams, Stephen L" uniqKey="Abrams S" first="Stephen L" last="Abrams">Stephen L. Abrams</name>
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<author><name sortKey="Franklin, Richard A" sort="Franklin, Richard A" uniqKey="Franklin R" first="Richard A" last="Franklin">Richard A. Franklin</name>
</author>
<author><name sortKey="Montalto, Giuseppe" sort="Montalto, Giuseppe" uniqKey="Montalto G" first="Giuseppe" last="Montalto">Giuseppe Montalto</name>
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<author><name sortKey="Cervello, Melchiorre" sort="Cervello, Melchiorre" uniqKey="Cervello M" first="Melchiorre" last="Cervello">Melchiorre Cervello</name>
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<author><name sortKey="Libra, Massimo" sort="Libra, Massimo" uniqKey="Libra M" first="Massimo" last="Libra">Massimo Libra</name>
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<author><name sortKey="Candido, Saverio" sort="Candido, Saverio" uniqKey="Candido S" first="Saverio" last="Candido">Saverio Candido</name>
</author>
<author><name sortKey="Malaponte, Grazia" sort="Malaponte, Grazia" uniqKey="Malaponte G" first="Grazia" last="Malaponte">Grazia Malaponte</name>
</author>
<author><name sortKey="Mazzarino, Maria C" sort="Mazzarino, Maria C" uniqKey="Mazzarino M" first="Maria C" last="Mazzarino">Maria C. Mazzarino</name>
</author>
<author><name sortKey="Fagone, Paolo" sort="Fagone, Paolo" uniqKey="Fagone P" first="Paolo" last="Fagone">Paolo Fagone</name>
</author>
<author><name sortKey="Nicoletti, Ferdinando" sort="Nicoletti, Ferdinando" uniqKey="Nicoletti F" first="Ferdinando" last="Nicoletti">Ferdinando Nicoletti</name>
</author>
<author><name sortKey="B Secke, Jorg" sort="B Secke, Jorg" uniqKey="B Secke J" first="Jörg" last="B Secke">Jörg B Secke</name>
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<author><name sortKey="Mijatovic, Sanja" sort="Mijatovic, Sanja" uniqKey="Mijatovic S" first="Sanja" last="Mijatovic">Sanja Mijatovic</name>
</author>
<author><name sortKey="Maksimovic Ivanic, Danijela" sort="Maksimovic Ivanic, Danijela" uniqKey="Maksimovic Ivanic D" first="Danijela" last="Maksimovic-Ivanic">Danijela Maksimovic-Ivanic</name>
</author>
<author><name sortKey="Milella, Michele" sort="Milella, Michele" uniqKey="Milella M" first="Michele" last="Milella">Michele Milella</name>
</author>
<author><name sortKey="Tafuri, Agostino" sort="Tafuri, Agostino" uniqKey="Tafuri A" first="Agostino" last="Tafuri">Agostino Tafuri</name>
</author>
<author><name sortKey="Chiarini, Francesca" sort="Chiarini, Francesca" uniqKey="Chiarini F" first="Francesca" last="Chiarini">Francesca Chiarini</name>
</author>
<author><name sortKey="Evangelisti, Camilla" sort="Evangelisti, Camilla" uniqKey="Evangelisti C" first="Camilla" last="Evangelisti">Camilla Evangelisti</name>
</author>
<author><name sortKey="Cocco, Lucio" sort="Cocco, Lucio" uniqKey="Cocco L" first="Lucio" last="Cocco">Lucio Cocco</name>
</author>
<author><name sortKey="Martelli, Alberto M" sort="Martelli, Alberto M" uniqKey="Martelli A" first="Alberto M" last="Martelli">Alberto M. Martelli</name>
</author>
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<series><title level="j">Oncotarget</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Agents (therapeutic use)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Drug Resistance, Neoplasm (MeSH)</term>
<term>Extracellular Signal-Regulated MAP Kinases (antagonists & inhibitors)</term>
<term>Extracellular Signal-Regulated MAP Kinases (genetics)</term>
<term>Humans (MeSH)</term>
<term>MAP Kinase Kinase Kinases (antagonists & inhibitors)</term>
<term>MAP Kinase Kinase Kinases (genetics)</term>
<term>Mutation (genetics)</term>
<term>Neoplasms (drug therapy)</term>
<term>Neoplasms (genetics)</term>
<term>Neoplasms (pathology)</term>
<term>PTEN Phosphohydrolase (antagonists & inhibitors)</term>
<term>PTEN Phosphohydrolase (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphoinositide-3 Kinase Inhibitors (MeSH)</term>
<term>Proto-Oncogene Proteins B-raf (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins B-raf (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>ras Proteins (antagonists & inhibitors)</term>
<term>ras Proteins (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques (usage thérapeutique)</term>
<term>Extracellular Signal-Regulated MAP Kinases (antagonistes et inhibiteurs)</term>
<term>Extracellular Signal-Regulated MAP Kinases (génétique)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>MAP Kinase Kinase Kinases (antagonistes et inhibiteurs)</term>
<term>MAP Kinase Kinase Kinases (génétique)</term>
<term>Mutation (génétique)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphohydrolase PTEN (antagonistes et inhibiteurs)</term>
<term>Phosphohydrolase PTEN (génétique)</term>
<term>Protéines G ras (antagonistes et inhibiteurs)</term>
<term>Protéines G ras (génétique)</term>
<term>Protéines proto-oncogènes B-raf (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes B-raf (génétique)</term>
<term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Résistance aux médicaments antinéoplasiques (MeSH)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Transduction du signal (MeSH)</term>
<term>Tumeurs (anatomopathologie)</term>
<term>Tumeurs (génétique)</term>
<term>Tumeurs (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>MAP Kinase Kinase Kinases</term>
<term>PTEN Phosphohydrolase</term>
<term>Proto-Oncogene Proteins B-raf</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
<term>ras Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>MAP Kinase Kinase Kinases</term>
<term>PTEN Phosphohydrolase</term>
<term>Proto-Oncogene Proteins B-raf</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
<term>ras Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>MAP Kinase Kinase Kinases</term>
<term>Phosphohydrolase PTEN</term>
<term>Protéines G ras</term>
<term>Protéines proto-oncogènes B-raf</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term>
<term>Neoplasms</term>
<term>Phosphatidylinositol 3-Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>MAP Kinase Kinase Kinases</term>
<term>Mutation</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Phosphohydrolase PTEN</term>
<term>Protéines G ras</term>
<term>Protéines proto-oncogènes B-raf</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Drug Resistance, Neoplasm</term>
<term>Humans</term>
<term>Phosphoinositide-3 Kinase Inhibitors</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23085539</PMID>
<DateCompleted><Year>2013</Year>
<Month>02</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>3</Volume>
<Issue>10</Issue>
<PubDate><Year>2012</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.</ArticleTitle>
<Pagination><MedlinePgn>1068-111</MedlinePgn>
</Pagination>
<Abstract><AbstractText>The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McCubrey</LastName>
<ForeName>James A</ForeName>
<Initials>JA</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Steelman</LastName>
<ForeName>Linda S</ForeName>
<Initials>LS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chappell</LastName>
<ForeName>William H</ForeName>
<Initials>WH</Initials>
</Author>
<Author ValidYN="Y"><LastName>Abrams</LastName>
<ForeName>Stephen L</ForeName>
<Initials>SL</Initials>
</Author>
<Author ValidYN="Y"><LastName>Franklin</LastName>
<ForeName>Richard A</ForeName>
<Initials>RA</Initials>
</Author>
<Author ValidYN="Y"><LastName>Montalto</LastName>
<ForeName>Giuseppe</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Cervello</LastName>
<ForeName>Melchiorre</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Libra</LastName>
<ForeName>Massimo</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Candido</LastName>
<ForeName>Saverio</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Malaponte</LastName>
<ForeName>Grazia</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mazzarino</LastName>
<ForeName>Maria C</ForeName>
<Initials>MC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Fagone</LastName>
<ForeName>Paolo</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Nicoletti</LastName>
<ForeName>Ferdinando</ForeName>
<Initials>F</Initials>
</Author>
<Author ValidYN="Y"><LastName>Bäsecke</LastName>
<ForeName>Jörg</ForeName>
<Initials>J</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mijatovic</LastName>
<ForeName>Sanja</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Maksimovic-Ivanic</LastName>
<ForeName>Danijela</ForeName>
<Initials>D</Initials>
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.

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